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(Circulation. 2005;111:2257-2273.)
© 2005 American Heart Association, Inc.
Basic Science for Clinicians |
From the Division of Cardiology & Cardiovascular Imaging Core Laboratories, University of Florida, Shands-Jacksonville, Jacksonville, Fla (M.A.C.), and the Cardiovascular Division, Brigham and Womens Hospital, Harvard Medical School, Boston, Mass (D.I.S.).
Correspondence to Daniel I. Simon, MD, Cardiovascular Division, 75 Francis St, Tower 3, Boston, MA 02115. E-mail dsimon@rics.bwh.harvard.edu
Key Words: stents restenosis inflammation prevention cells
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
| Introduction |
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Resolution of restenosis probably requires both creation of the largest possible residual lumen and substantial inhibition of intimal hyperplasia. J.S. Forrester and coworkers1
Dr Forresters prediction that resolution of restenosis would require the translational merging of molecular mechanisms of proliferation with local scaffolding and drug-delivery devices appears to have been remarkably prescient. The application of drug-eluting stent (DES) technology to improve clinical outcomes after percutaneous coronary intervention (PCI) represents one of the greatest success stories in cardiology. This review highlights the molecular basis of restenosis and DES for the clinical and interventional cardiologist and vascular biologist.
| Restenosis: Definitions and Mechanisms |
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